Key result
In murine models of viral myocarditis, the absence of tyrosine kinase p56lck allows the host to achieve 100% survival with limited viral replication.
Understanding the molecular mechanisms of viral myocarditis, particularly the role of p56lck and downstream targets, provides potential future therapeutic targets for heart failure.
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p56lck remains a preclinical target in viral myocarditis; leaves open translation to human heart failure therapies.
P LIU (2002) conducted a review in Viral myocarditis. In murine models of viral myocarditis, the absence of tyrosine kinase p56lck allows the host to achieve 100% survival with limited viral replication.
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